Abstract
Background Cardiovascular (CV) disease is one of the main causes of mortality in axial spondyloarthritis (axSpA). The higher incidence of CV risk factors and systemic chronic inflammation increase CV risk in axSpA.1 This is enhanced by a dysregulation of adipokines. Low levels of omentin, an anti-inflammatory adipokine, have been associated with metabolic dysfunction and CV disease in general population and conditions different from axSpA.2,3 Objectives To evaluate the implication of omentin in CV risk and subclinical atherosclerosis in axSpA at the genetic and functional (mRNA and protein) level. Methods 382 patients fulfilling the ASAS classification criteria for axSpA4 and 84 controls were included. Carotid ultrasound was performed to evaluate the presence of subclinical atherosclerosis. Serum omentin levels were assessed by ELISA. mRNA expression of ITLN1, coding omentin, was evaluated by RT-qPCR. ITLN1 rs12409609 (C/T), in complete linkage disequilibrium with a polymorphism previously associated with coronary artery disease,5 was genotyped by TaqMan probes. Results were adjusted by potential confounding factors (STATA® v.11.1). Results Serum and mRNA levels of omentin were lower in axSpA compared to controls (p Conclusion style=”font-family: ‘Times New Roman’,’serif’; font-size: 10.0pt; margin: 0cm; margin-bottom: 8.0pt; line-height: 106%; margin-left: 0cm; margin-right: 0cm; margin-top: 0cm; mso-style-name: Normal_0; text-align: justify;” fontsize=”11.0” data-pos-index=”15” class-name=”Deleted”>Omentin is linked to obesity and adverse lipid profiles in axSpA. Additionally, low serum levels of omentin are associated with the presence of IBD in axSpA. These data support a role of omentin as a CV risk biomarker in axSpA.
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